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The differences we found between the treatment and control mice were partly due to telomere shortening in infected animals, and, somewhat surprisingly, telomere elongation in sham-controls (which we have observed previously [5]).
18 We showed that the suppressive effects of apocynin treatment on intestinal polyp formation in Min mice were partly explained by the suppression of iNOS.
As expected, GF mice were partly protected against lard-induced WAT inflammation, although the protection against obesity in GF mice was less than that observed in previous studies (Bäckhed et al., 2007; Caesar et al., 2012; Ding et al., 2010; Rabot et al., 2010).
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We next determined whether the anti-tumor effect of PX-866 in KrasLA1 mice was partly due to inhibition of BASC expansion.
These results suggest that the alteration of GSK3β function affected mood-behavior in mice, and the lithium-sensitive excitatory mood behaviors of DGKβ KO mice are partly caused by the reduced phosphorylation levels of Akt and GSK3β.
Since the severity of colitis symptoms in mice is partly dependent on the DSS dose [10], [23], we hypothesized that a higher dose of DSS might induce a comparable accumulation of pDCs in MLNs of WT animals.
Additional studies have shown that the neuroprotective effects observed in calorie restricted mice is partly due to downregulation of miRNAs that target the pro-survival gene Bcl-2 [ 28].
For example, the behavioral phenotype of adult 5-HTT knock-out mice is partly driven by altered 5-HT function during a critical period of development rather than ongoing changes in 5-HT in the adult (Ansorge et al. 2004).
90 The resistance to EAE in IL-1 deficient IL-1 deficienty attributed to inefficient generation of Th1 and Th17 T cell responses; and previous results have shown that IL-1 synthesis by APCs is necessary to facilitate efficient T cell interactions by enhancing T cell expression of CD154 (CD40L) and CD134 (OX40) to induce TNF-α synthesis and adaptive imicee maturation.
The accelerated aging phenotype of Zmpste24 −/− mouse was partly alleviated when crossed into a p53-deficient background [ 40] and completely rescued when made heterozygous for Lmna expression revealing a dosage effect of pre-laminA on the pathology [ 40].
As depicted in Fig 5A, glucose tolerance was impaired in FasF/F mice, whereas FasΔmye littermates were partly protected from LPS-induced deterioration of glucose metabolism.
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